18beta-glycyrrhetinic acid induces ROS-mediated apoptosis to ameliorate hepatic fibrosis by targeting PRDX1/2 in activated HSCs

Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis. 18beta-glycyrrhetinic acid (18β-GA) is a natural compound that exists widely in herbal medicines, such as Glycyrrhiza uralensis Fisch, which is...

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Published inJournal of pharmaceutical analysis Vol. 12; no. 4; pp. 570 - 582
Main Authors Zhang, Qian, Luo, Piao, Zheng, Liuhai, Chen, Jiayun, Zhang, Junzhe, Tang, Huan, Liu, Dandan, He, Xueling, Shi, Qiaoli, Gu, Liwei, Li, Jiahao, Guo, Qiuyan, Yang, Chuanbin, Wong, Yin Kwan, Xia, Fei, Wang, Jigang
Format Journal Article
LanguageEnglish
Published Xi'an Elsevier B.V 01.08.2022
Xi'an Jiaotong University, Journal of Pharmaceutical Analysis
Artemisinin Research Center and Institute of Chinese Materia Medica,Chinese Academy of Chinese Medical Sciences,Beijing,100700,China
Department of Geriatrics,Shenzhen People's Hospital(The Second Clinical Medical College,Jinan University),Shenzhen,518020,China%Department of Geriatrics,Shenzhen People's Hospital(The Second Clinical Medical College,Jinan University),Shenzhen,518020,China%Artemisinin Research Center and Institute of Chinese Materia Medica,Chinese Academy of Chinese Medical Sciences,Beijing,100700,China%Department of Biological Sciences,National University of Singapore,Singapore,117543,Singapore
Xi'an Jiaotong University
Subjects
Acids
Actin
Apoptosis
Chromatography
Collagen
Collagen (type I)
Enzymatic activity
Fibrosis
Flow cytometry
Glycyrrhetinic acid
Hepatic fibrosis
Hepatitis
Herbal medicine
Laboratory animals
Liver
Liver diseases
Metabolism
Metabolites
Molecular modelling
Original
Pathogenesis
Peroxiredoxin
Proteins
Reactive oxygen species
Smooth muscle
Stellate cells
Surface plasmon resonance
United States > US
China
Hepatic fibrosis
Peroxiredoxin
Reactive oxygen species
Glycyrrhetinic acid
Apoptosis
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Abstract Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis. 18beta-glycyrrhetinic acid (18β-GA) is a natural compound that exists widely in herbal medicines, such as Glycyrrhiza uralensis Fisch, which is used for treating multiple liver diseases, especially in Asia. In the present study, we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs. 18β-GA inhibited the expression of α-smooth muscle actin and collagen type I alpha-1. Using a chemoproteomic approach derived from activity-based protein profiling, together with cellular thermal shift assay and surface plasmon resonance, we found that 18β-GA covalently targeted peroxiredoxin 1 (PRDX1) and peroxiredoxin 2 (PRDX2) proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities. 18β-GA induced the elevation of reactive oxygen species (ROS), resulting in the apoptosis of activated HSCs. PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs. Collectively, our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis, highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis. [Display omitted] •18β-GA ameliorates hepatic fibrosis and inhibits ECM deposition.•18β-GA directly targets PRDX1 and PRDX2 in activated HSCs.•18β-GA binding to the cysteines of PRDX1 and PRDX2 inhibits their enzyme activities.•18β-GA induces ROS-mediated activated-HSC apoptosis by targeting PRDX1 and PRDX2.
AbstractList Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis. 18beta-glycyrrhetinic acid (18β-GA) is a natural compound that exists widely in herbal medicines, such as Glycyrrhiza uralensis Fisch, which is used for treating multiple liver diseases, especially in Asia. In the present study, we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs. 18β-GA inhibited the expression of α-smooth muscle actin and collagen type I alpha-1. Using a chemoproteomic approach derived from activity-based protein profiling, together with cellular thermal shift assay and surface plasmon resonance, we found that 18β-GA covalently targeted peroxiredoxin 1 (PRDX1) and peroxiredoxin 2 (PRDX2) proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities. 18β-GA induced the elevation of reactive oxygen species (ROS), resulting in the apoptosis of activated HSCs. PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs. Collectively, our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis, highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis. Image 1 • 18β-GA ameliorates hepatic fibrosis and inhibits ECM deposition. • 18β-GA directly targets PRDX1 and PRDX2 in activated HSCs. • 18β-GA binding to the cysteines of PRDX1 and PRDX2 inhibits their enzyme activities. • 18β-GA induces ROS-mediated activated-HSC apoptosis by targeting PRDX1 and PRDX2.
Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis. 18beta-glycyrrhetinic acid (18ß-GA) is a natural compound that exists widely in herbal medicines, such as Glycyrrhiza uralensis Fisch, which is used for treating multiple liver diseases, especially in Asia. In the present study, we demonstrated that 18ß-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs. 18ß-GA inhibited the expression of a-smooth muscle actin and collagen type I alpha-1. Using a chemoproteomic approach derived from activity-based protein profiling, together with cellular thermal shift assay and surface plasmon resonance, we found that 18ß-GA covalently targeted peroxiredoxin 1 (PRDX1) and peroxiredoxin 2 (PRDX2) proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities. 18ß-GA induced the elevation of reactive oxygen species (ROS), resulting in the apoptosis of activated HSCs. PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs. Collectively, our findings revealed the target proteins and molecular mechanisms of 18ß-GA in ameliorating hepatic fibrosis, highlighting the future development of 18ß-GA as a novel therapeutic drug for hepatic fibrosis.
Hepatic stellate cells(HSCs)are essential drivers of fibrogenesis.Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis.18beta-glycyrrhetinic acid(18β-GA)is a natural com-pound that exists widely in herbal medicines,such as Glycyrrhiza uralensis Fisch,which is used for treating multiple liver diseases,especially in Asia.In the present study,we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs.18β-GA inhibited the expression of α-smooth muscle actin and collagen type Ⅰ alpha-1.Using a chemoproteomic approach derived from activity-based protein profiling,together with cellular thermal shift assay and surface plasmon reso-nance,we found that 18β-GA covalently targeted peroxiredoxin 1(PRDX1)and peroxiredoxin 2(PRDX2)proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities.18β-GA induced the elevation of reactive oxygen species(ROS),resulting in the apoptosis of activated HSCs.PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs.Collectively,our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis,highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis.
Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis. 18beta-glycyrrhetinic acid (18β-GA) is a natural compound that exists widely in herbal medicines, such as Glycyrrhiza uralensis Fisch, which is used for treating multiple liver diseases, especially in Asia. In the present study, we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs. 18β-GA inhibited the expression of α-smooth muscle actin and collagen type I alpha-1. Using a chemoproteomic approach derived from activity-based protein profiling, together with cellular thermal shift assay and surface plasmon resonance, we found that 18β-GA covalently targeted peroxiredoxin 1 (PRDX1) and peroxiredoxin 2 (PRDX2) proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities. 18β-GA induced the elevation of reactive oxygen species (ROS), resulting in the apoptosis of activated HSCs. PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs. Collectively, our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis, highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis. [Display omitted] •18β-GA ameliorates hepatic fibrosis and inhibits ECM deposition.•18β-GA directly targets PRDX1 and PRDX2 in activated HSCs.•18β-GA binding to the cysteines of PRDX1 and PRDX2 inhibits their enzyme activities.•18β-GA induces ROS-mediated activated-HSC apoptosis by targeting PRDX1 and PRDX2.
Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis. 18beta-glycyrrhetinic acid (18β-GA) is a natural compound that exists widely in herbal medicines, such as Glycyrrhiza uralensis Fisch, which is used for treating multiple liver diseases, especially in Asia. In the present study, we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs. 18β-GA inhibited the expression of α-smooth muscle actin and collagen type I alpha-1. Using a chemoproteomic approach derived from activity-based protein profiling, together with cellular thermal shift assay and surface plasmon resonance, we found that 18β-GA covalently targeted peroxiredoxin 1 (PRDX1) and peroxiredoxin 2 (PRDX2) proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities. 18β-GA induced the elevation of reactive oxygen species (ROS), resulting in the apoptosis of activated HSCs. PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs. Collectively, our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis, highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis.Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis. 18beta-glycyrrhetinic acid (18β-GA) is a natural compound that exists widely in herbal medicines, such as Glycyrrhiza uralensis Fisch, which is used for treating multiple liver diseases, especially in Asia. In the present study, we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs. 18β-GA inhibited the expression of α-smooth muscle actin and collagen type I alpha-1. Using a chemoproteomic approach derived from activity-based protein profiling, together with cellular thermal shift assay and surface plasmon resonance, we found that 18β-GA covalently targeted peroxiredoxin 1 (PRDX1) and peroxiredoxin 2 (PRDX2) proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities. 18β-GA induced the elevation of reactive oxygen species (ROS), resulting in the apoptosis of activated HSCs. PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs. Collectively, our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis, highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis.
Author Guo, Qiuyan
Wong, Yin Kwan
Zhang, Qian
Zheng, Liuhai
He, Xueling
Luo, Piao
Chen, Jiayun
Gu, Liwei
Tang, Huan
Yang, Chuanbin
Xia, Fei
Li, Jiahao
Zhang, Junzhe
Liu, Dandan
Shi, Qiaoli
Wang, Jigang
AuthorAffiliation Artemisinin Research Center and Institute of Chinese Materia Medica,Chinese Academy of Chinese Medical Sciences,Beijing,100700,China;Department of Geriatrics,Shenzhen People's Hospital(The Second Clinical Medical College,Jinan University),Shenzhen,518020,China%Department of Geriatrics,Shenzhen People's Hospital(The Second Clinical Medical College,Jinan University),Shenzhen,518020,China%Artemisinin Research Center and Institute of Chinese Materia Medica,Chinese Academy of Chinese Medical Sciences,Beijing,100700,China%Department of Biological Sciences,National University of Singapore,Singapore,117543,Singapore
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ContentType Journal Article
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Copyright Xi'an Jiaotong University, Journal of Pharmaceutical Analysis Aug 2022
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Issue 4
Keywords Hepatic fibrosis
Peroxiredoxin
Reactive oxygen species
Glycyrrhetinic acid
Apoptosis
Language English
License This is an open access article under the CC BY-NC-ND license.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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content type line 23
Both authors contributed equally to this work.
ORCID 0000-0002-5862-2190
0000-0002-0575-0105
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  year: 2022
  text: 2022-08-01
  day: 01
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PublicationPlace Xi'an
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PublicationTitle Journal of pharmaceutical analysis
PublicationTitle_FL Journal of Pharmaceutical Analysis
PublicationYear 2022
Publisher Elsevier B.V
Xi'an Jiaotong University, Journal of Pharmaceutical Analysis
Artemisinin Research Center and Institute of Chinese Materia Medica,Chinese Academy of Chinese Medical Sciences,Beijing,100700,China
Department of Geriatrics,Shenzhen People's Hospital(The Second Clinical Medical College,Jinan University),Shenzhen,518020,China%Department of Geriatrics,Shenzhen People's Hospital(The Second Clinical Medical College,Jinan University),Shenzhen,518020,China%Artemisinin Research Center and Institute of Chinese Materia Medica,Chinese Academy of Chinese Medical Sciences,Beijing,100700,China%Department of Biological Sciences,National University of Singapore,Singapore,117543,Singapore
Xi'an Jiaotong University
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– name: Artemisinin Research Center and Institute of Chinese Materia Medica,Chinese Academy of Chinese Medical Sciences,Beijing,100700,China
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– name: Xi'an Jiaotong University
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Snippet Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis....
Hepatic stellate cells (HSCs) are essential drivers of fibrogenesis. Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis....
Hepatic stellate cells(HSCs)are essential drivers of fibrogenesis.Inducing activated-HSC apoptosis is a promising strategy for treating hepatic...
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SubjectTerms Acids
Actin
Apoptosis
Chromatography
Collagen
Collagen (type I)
Enzymatic activity
Fibrosis
Flow cytometry
Glycyrrhetinic acid
Hepatic fibrosis
Hepatitis
Herbal medicine
Laboratory animals
Liver
Liver diseases
Metabolism
Metabolites
Molecular modelling
Original
Pathogenesis
Peroxiredoxin
Proteins
Reactive oxygen species
Smooth muscle
Stellate cells
Surface plasmon resonance
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Title 18beta-glycyrrhetinic acid induces ROS-mediated apoptosis to ameliorate hepatic fibrosis by targeting PRDX1/2 in activated HSCs
URI https://dx.doi.org/10.1016/j.jpha.2022.06.001
https://www.proquest.com/docview/2729566031
https://www.proquest.com/docview/2714656596
https://d.wanfangdata.com.cn/periodical/ywfxxb-e202204005
https://pubmed.ncbi.nlm.nih.gov/PMC9463498
Volume 12
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